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Article: Formation of Kiss1R/GPER Heterocomplexes Negatively Regulates Kiss1R-mediated Signalling through Limiting Receptor Cell Surface Expression

TitleFormation of Kiss1R/GPER Heterocomplexes Negatively Regulates Kiss1R-mediated Signalling through Limiting Receptor Cell Surface Expression
Authors
KeywordsGPCR dimerization
Kisspeptin receptor
G protein-coupled estrogen receptor
Cell signaling
Issue Date2021
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/jmb
Citation
Journal of Molecular Biology, 2021, v. 433 n. 7, article no. 166843 How to Cite?
AbstractKisspeptin receptor (Kiss1R) is an important receptor that plays central regulatory roles in reproduction by regulating hormone release in the hypothalamus. We hypothesize that the formation of heterocomplexes between Kiss1R and other hypothalamus G protein-coupled receptors (GPCRs) affects their cellular signaling. Through screening of potential interactions between Kiss1R and hypothalamus GPCRs, we identified G protein-coupled estrogen receptor (GPER) as one interaction partner of Kiss1R. Based on the recognised function of kisspeptin and estrogen in regulating the reproductive system, we investigated the Kiss1R/GPER heterocomplex in more detail and revealed that complex formation significantly reduced Kiss1R-mediated signaling. GPER did not directly antagonize Kiss1R conformational changes upon ligand binding, but it rather reduced the cell surface expression of Kiss1R. These results therefore demonstrate a regulatory mechanism of hypothalamic hormone receptors via receptor cooperation in the reproductive system and modulation of receptor sensitivity.
Persistent Identifierhttp://hdl.handle.net/10722/305124
ISSN
2023 Impact Factor: 4.7
2023 SCImago Journal Rankings: 2.212
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKe, R-
dc.contributor.authorLok, SIS-
dc.contributor.authorSingh, K-
dc.contributor.authorChow, BKC-
dc.contributor.authorJanovjak, H-
dc.contributor.authorLee, LTO-
dc.date.accessioned2021-10-05T02:40:04Z-
dc.date.available2021-10-05T02:40:04Z-
dc.date.issued2021-
dc.identifier.citationJournal of Molecular Biology, 2021, v. 433 n. 7, article no. 166843-
dc.identifier.issn0022-2836-
dc.identifier.urihttp://hdl.handle.net/10722/305124-
dc.description.abstractKisspeptin receptor (Kiss1R) is an important receptor that plays central regulatory roles in reproduction by regulating hormone release in the hypothalamus. We hypothesize that the formation of heterocomplexes between Kiss1R and other hypothalamus G protein-coupled receptors (GPCRs) affects their cellular signaling. Through screening of potential interactions between Kiss1R and hypothalamus GPCRs, we identified G protein-coupled estrogen receptor (GPER) as one interaction partner of Kiss1R. Based on the recognised function of kisspeptin and estrogen in regulating the reproductive system, we investigated the Kiss1R/GPER heterocomplex in more detail and revealed that complex formation significantly reduced Kiss1R-mediated signaling. GPER did not directly antagonize Kiss1R conformational changes upon ligand binding, but it rather reduced the cell surface expression of Kiss1R. These results therefore demonstrate a regulatory mechanism of hypothalamic hormone receptors via receptor cooperation in the reproductive system and modulation of receptor sensitivity.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/jmb-
dc.relation.ispartofJournal of Molecular Biology-
dc.subjectGPCR dimerization-
dc.subjectKisspeptin receptor-
dc.subjectG protein-coupled estrogen receptor-
dc.subjectCell signaling-
dc.titleFormation of Kiss1R/GPER Heterocomplexes Negatively Regulates Kiss1R-mediated Signalling through Limiting Receptor Cell Surface Expression-
dc.typeArticle-
dc.identifier.emailChow, BKC: bkcc@hku.hk-
dc.identifier.authorityChow, BKC=rp00681-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jmb.2021.166843-
dc.identifier.pmid33539880-
dc.identifier.scopuseid_2-s2.0-85100681944-
dc.identifier.hkuros326283-
dc.identifier.volume433-
dc.identifier.issue7-
dc.identifier.spagearticle no. 166843-
dc.identifier.epagearticle no. 166843-
dc.identifier.isiWOS:000630007900006-
dc.publisher.placeUnited Kingdom-

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